Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The IGF regulatory system has been shown to mediate mitogenic effects during normal growth and tumor proliferation. The bioavailability of both IGF-I and IGF-II is regulated by at least six specific IGF binding proteins (IGFBPs). Whereas IGFBP-3 is the main IGFBP postnatally, IGFBP-2 is the predominant IGFBP during fetal life. In addition, IGFBP-2 is expressed in a range of tumor cell lines. In order to investigate the IGF regulatory pathway in malignancies we analyzed by RIA serum samples of 49 children with leukemia, Non-Hodgkins' Lymphoma (NHL) or solid tumors at the time of diagnosis. Serum concentrations of IGF-I (mean/range: -2.4/0.3 to -9.9 SDS), IGF-II (-2.5/0.2 to -5.6 SDS) and IGFBP-3 (-1.3/2.2 to -6.8 SDS) were significantly decreased, but IGFBP-2 (3.2/-0.9 to 8.6 SDS) was elevated. Both absolute as well as SDS values of IGF-I, -II and the sum of IGF-I and IGF-II (r = -0.49, p < 0.01) were inversely correlated with IGFBP-2. Serum levels of the growth factors IGF-I and IGF-II were significantly decreased in different types of malignancies to concentrations usually seen only in patients with growth hormone deficiency or during starvation. However, the elevated levels of IGFBP-2 in 70% of our patients exceeded by far those in growth hormone deficiency. Furthermore, in this study we could demonstrate that serum levels of IGF-I and IGF-II were inversely correlated to IGFBP-2 independent on the type of malignancy, indicating a common regulatory mechanism of the IGF signaling pathway in these diseases.
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PMID:[Serum concentrations of insulin-like growth factors (IGF)-I and IGF-II and IGF binding proteins (IGFBP)-2 and IGFBP-3 in 49 children with ALL, NHL or solid tumors]. 756 58

In 1963, Prader, Tanner, and von Harnack published a landmark article describing catch-up growth in children after illness or starvation. That same year, Tanner proposed a theory about catch-up growth based on a central regulatory principle that is 'informed' about an organism's height by means of a humoral factor. This led to the assumption that, when dissociation between a central age-appropriate set point for body size and actual body size occurs, an efferent signal is transmitted to growth tissue to stimulate growth that corresponds to age-appropriate body size. Catch-up growth has been observed in a wide range of endocrinological, nutritional, medical, and emotional disturbances, and the underlying causes are complex and not always well understood. Recently, catch-up growth in four situations has attracted the attention of endocrinologists, as these situations provide useful lessons for the clinician: hypothyroidism, growth hormone deficiency, intrauterine growth retardation, and adoption of children born in developing countries and raised in Western societies.
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PMID:Catch-up growth: new lessons for the clinician. 1251 Sep 76